Analgesics for oral surgery in dogs and cats - DVM
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Analgesics for oral surgery in dogs and cats


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Hyperthermia in cats with the use of opiates is predictable and therefore monitoring is essential. Patients should be monitored during the anesthetic period and up to five hours during post procedure. If hyperthermia becomes significant, reversal agents that are mu antagonists can be administered. Butorphanol and nalbuphine are kappa-receptor agonists. That property provides some residual analgesia when they are used as mu antagonists to reverse morphine. Naloxone is an antagonist at the mu, kappa and gamma receptors, so administration of this reversal agent provides no residual analgesia.

Morphine, in particular, will cause vomiting in a significant number of patients. A decrease in incidence occurs with intravenous administration. Histamine release is a problem with rapid administration, so morphine given IV must be given slowly over a period of 30 seconds. An alternative to morphine in cats is hydromorphone that is an excellent analgesic in this species. Intravenous administration of hydromorphone in cats provides quicker onset, increased intensity and longer duration with a decreased incidence of vomiting than IM or SQ administration. Again, hyperthermia is a concern, so monitoring temperature is essential.

Oral-surgery patients may be painful and difficult to medicate post-operatively per os. Fentanyl transdermal patches are viable options for managing postoperative pain in dogs and cats undergoing oral surgical procedures. The onset of effect in dogs and cats is 18 to 24 hours and six to 12 hours, respectively. If using fentanyl patches, the void between placement and onset of action should be adequately covered with additional analgesics.

Butorphanol is an mu antagonist allowing for only minimal control of somatic pain. It is expensive and frequent dosing is required due to its short half-life. Consequently it is a poor choice for managing pain associated with oral surgery.

Buprenorphine has partial agonist activity at the mu receptor and consequently less profound analgesic properties than would a pure agonist. However, it is a safe and effective analgesic and is a great option for use in cats sublingually and transdermally. It is a good choice when anticipating mild to moderate postoperative pain.

Cox-2 Selective NSAIDs

The breakdown of arachidonic acid by cyclooxygenase (Cox) enzymes produces prostaglandins. These proinflammatory compounds are released from various cell types at the site of tissue injury. Other compounds, including cytokines and growth factors, aid in stimulating the production of additional prostaglandins. Prostaglandins sensitize afferent neurons to noxious chemical, thermal and mechanical stimuli and play a major role in the process of maintaining inflammation.

Prostaglandins are involved at the site of inflammation and play a significant role at the spinal level. Peripheral inflammation upregulates cyclooxygenase enzyme expression in the spinal cord. Therefore, drugs that can prevent the prostaglandin production can be used to decrease this phenomenon. This may be particularly effective when given preoperatively prior to surgical stimulation.

The non-steroidal anti-inflammatory drugs (NSAIDs) inhibit Cox enzymes. Their use allows for effective treatment of pain and hyperalgesia associated with inflammation. Cyclooxygenase-2 (Cox-2) selective NSAIDs have been widely used in veterinary medicine as analgesics. Adverse effects consistently experienced with earlier NSAIDs are nowhere near as significant with these newer agents. Adverse effects are still possible, however. NSAIDs as sole agents for analgesia can be effective; however, using multiple agents in a multimodal approach offers safety and efficacy beyond that of single agents. An NSAID in combination with an opiate in humans has demonstrated opioid sparing effects in the range of 20 percent to 30 percent. To date no Cox-2 selective NSAID approved for use in veterinary medicine has been shown to demonstrate significant advantages over another.

5-Lox selective NSAIDs

Arachidonic acid breakdown by 5-lipoxygenase (5-Lox) produces leukotrienes that, like prostaglandins, significantly affect the inflammatory process. Both classes work together, synergistically potentiating the inflammatory cascade. The combination of Cox-2 and 5-Lox pathway inhibition could theoretically enhance the anti-inflammatory effect on tissue. The NSAID tepoxalin, approved for use in dogs, demonstrates Cox-1, Cox-2 and 5-Lox inhibition. This agent has not been shown to demonstrate significant advantages over Cox-2 inhibition alone and bleeding may be an issue due to its Cox-1 effect.


Source: DVM360 MAGAZINE,
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